Runt-Related Transcription Factor 2 (RUNX2) ELISA Kits

Human Runt-Related Transcription Factor 2 (RUNX2) interaction partners

1. We performed histomorphometric analyses, and we quantified the expression levels of the osteogenic transcription factor RUNX2 in circulating mesenchymal stem cells in acromegalic patients. Our results showed an abnormal microarchitecture and demonstrated that bone impairment in these patients is associated with the upregulation of RUNX2 expression.

2. Thus, PTH stimulated the expression of lnc-SUPT3H-1:16, miR-6797-5p and Runx2, and due to the sponging mechanism of lnc- SUPT3H-1:16 towards miR-6797-5p, Runx2 was protected, resulting in the promotion of osteoblast differentiation.

3. RUNX2 gene transcription is regulated by the methylation status of specific CpG sites in the promoter and may determine RUNX2 availability in OA cartilage for transactivation of genes such as MMP13.

4. Overexpression of Runx2 gene was beneficial for osteogenic differentiation of HUVECs, while overexpression of osterix gene did not show osteogenic differential potential.

5. Mechanism of TRbeta repression of oncogenic gene expression: TRbeta recruitment of BRG1 induces chromatin compaction and diminishes RUNX2 expression. Therefore, BRG1-mediated chromatin remodeling may be obligatory for TRbeta transcriptional repression and tumor suppressor function in thyroid tumorigenesis.

6. All these findings indicate that RUNX2 mutation can reduce the osteogenic capacity of dental follicle cells through inhibiting osteoblast-associated genes, thereby disturbing alveolar bone formation, which serves as a motive force for tooth eruption

7. these data indicated that miR-23b was involved in TNF-alpha-mediated reduction of bone marrow mesenchymal stem cell osteogenesis by targeting runx2.

8. that cross-talk between cAMP/PKA signaling and RUNX2 promotes a malignant phenotype of glioma cells

9. Study identified RUNX2 to be targeted by miR-217 which directly bound to RUNX2 mRNA and inhibited its expression in bladder cancer cells. Also, findings demonstrated that RUNX2 expression was upregulated by hsa_circ_0000144. Moreover, rescue assays demonstrated that RUNX2 was a downstream effector molecule of hsa_circ_0000144/miR-217 network. These results revealed the oncogenic role of RUNX2 in bladder neoplasm.

10. In summary, these results reveal that PTHLH expression is a poor prognosis marker in head and neck squamous cell carcinoma patients, and RUNX2-PTHLH axis contributes to head and neck squamous cell carcinoma tumor growth.

11. Knockdown of RUNX2 significantly inhibited TE-1 and EC-109 cell viability, repressed TE-1 cell migration and invasion, and increased TE-1 cell apoptosis and were associated with the activation of the PI3K/AKT and ERK pathways.

12. Results show that RUNX2 gene silencing increased gemcitabine (GEM) sensitivity of p53mutated pancreatic cancer (PaCa) MiaPaCa2 spheres suggesting that RUNX2 is involved in PaCa-GEM resistance in presence of mutated p53.

13. Runx2 overexpression effectively decreased TNF-alpha-induced Bax and cleaved caspase-3 expression levels

14. RUNX2 is one of the promising molecular targets for the treatment of the patients with pancreatic cancer regardless of their p53 status[review]

15. we identified a novel missense mutation of RUNX2 in 2 patients by Whole exome sequencing and showed potential correlations between facial phenotypes and missense mutations in Runt domain through a mini-meta analysis.

16. Mutant Runx2 regulates amelogenesis and osteogenesis through a miR-185-5p-Dlx2 axis.

17. Results show that RUNX2 is highly expressed in bladder cancer tissues and are negatively correlated with miR-154 levels. This is likely through miR-154 binding the 3'-UTR of RUNX2 mRNA, promoting its degradation.

18. Results identified a novel mutation besides the previously known in one patient with cleidocranial dysplasia (CCD). G462X mutation in exon 8 is located in the C-terminus of proline/serine/threonine-rich (PST) domain. It might reduce the Runx2 transacting activity, lower the protein stability, downgrade the expression of bone marker genes, and eventually diminish osteoblast differentiation in CCD patients.

19. Findings reveal a novel mechanism that Runx2 is transcriptionally regulated by HSP90 via the AKT/GSK-3beta/beta-catenin signaling pathway, and by which leads to apoptosis of osteosarcoma cells.

20. Increased baseline gene expressions of RUNX2, p21 and caspase 3 in the peripheral blood might predict better responses to methotrexate therapy.

Zebrafish Runt-Related Transcription Factor 2 (RUNX2) interaction partners

1. quantitative data on the kinetics of gene expression is presented; new splice forms reported

2. Runx2 may have an evolutionarily conserved role in axis formation

Mouse (Murine) Runt-Related Transcription Factor 2 (RUNX2) interaction partners

1. Upon Runx2 silencing, autophagy-related proteins and RANKL were repressed in osteoblasts, thereby potentially causing the tooth eruption disorder.

2. These results suggest a new mechanism whereby Smad4 controls chondrocyte hypertrophy by up-regulating Runx2 expression during skeletal development. The regulatory mechanism involving Smad4-mediated Runx2 activation uncovered here provides critical insights into bone development and pathogenesis of chondrodysplasia.

3. our results indicate that Runx2 is weakly expressed in the LepR(+) population without osteoblastic commitment, and the LepR(+)Runx2-GFP(low) stromal cells sit atop the BM stromal hierarchy.

4. Runx2+/- mice had defects in bone resorption, reduced circulating levels of bioactive osteocalcin, and reduced expression of osteocalcin's target genes in the brain. Consequently, they had significant impairment in cognitive function and increased anxiety-like behavior.

5. Findings suggest that inhibition of Runx2 in chondrocytes could at least partially rescue destabilization of the medial meniscus (DMM) surgery-induced osteoarthritis (OA)-like defects.

6. This study reveals that RUNX2 is differentially expressed in ATII cells vs. fibroblasts in lung fibrosis, which contributes to profibrotic cell function. Cell-specific targeting of RUNX2 pathways may represent a therapeutic approach for IPF.

7. we have identified novel interaction between p38 MAPK and Runx2 enhances Runx2 transactivity, thus promoting vascular smooth muscle cells calcification

8. By using microRNA array, we identified a large number of microRNAs that showed different expression between wild-type Runx2 group and mutant groups. The aim of this study is to find out the effect of mmu-miR-1963, which was downregulated in all mutant Runx2 groups, on the ameloblast differentiation of LS8 cells

9. Results indicate that Dlx5 and Runx2 are critical factors for the upregulated Osterix expression in shPP2A cells, which is considered to be important for the accelerated osteoblast differentiation in these cells.

10. the expression of mouse Amtn gene in amelogenesis is mediated by Runx2/Cbfbeta complex. Runx2/Cbfbeta can bind to the two Runx2 binding motifs AACCACT (-1342/-1336) and AACCAAA (-98/-92) in the Amtn promoter and regulate Amtn gene expression.

11. Mutant Runx2 regulates amelogenesis and osteogenesis through a miR-185-5p-Dlx2 axis.

12. Puerarin may promote MC3T3E1 osteoblastlike cell viability and differentiation, which may be related to the downregulation of miR204 and the following activation of Runx2.

13. mTOR/Raptor signaling is essential for bone formation in vivo through the regulation of Runx2 expression.

14. these findings provide evidence that Cx43 and Runx2 functionally intersect in vivo to regulate cortical bone properties and affect osteoblast differentiation and proliferation

15. miR-133a-5p targets the 3' UTR of RUNX2 mRNA to regulate the expression of RUNX2 negatively.

16. muramyl dipeptide directly augmented osteoblast differentiation and bone-forming gene expression by Runx2 activation.

17. Loss of Runx1 and Runx2 inhibits prostate cell motility.

18. fetal administration of Entinostat/MS-275, a class I histone deacetylase (HDAC)-specific inhibitor, partially prevents delayed closure of cranial sutures in Runx2(+/-) mice strain of C57BL/6J by two mechanisms: 1) posttranslational acetylation of Runx2 protein, which stabilized the protein and activated its transcriptional activity; and 2) epigenetic regulation of Runx2 and other bone marker genes

19. These data suggest that NaF promotes the osteoblastic differentiation of MC3T3-E1 cells through the Runx2/Osterix pathway and may be effective for the treatment of bone-related disorders.

20. results suggest that Edil3 may stimulate osteoblast differentiation and matrix mineralization by increasing expression of Runx2 through alpha5beta1 integrin /ERK pathway

Rabbit Runt-Related Transcription Factor 2 (RUNX2) interaction partners

1. The results suggest that gene therapy using Runx2-modi fi ed dental pulp stem cells was more effective during bone deposition and new bone formation in tibia Distraction osteogenesis.

2. Runx2-modified adipose-derived stem cells promote tendon graft integration in anterior cruciate ligament reconstruction.

3. The OPG expression levels decreased while those of RANKL and RUNX2 increased during orthodontic tooth movement, which suggested that they play a role in the osteogenesis process and the reconstruction of periodontal tissue.

Xenopus laevis Runt-Related Transcription Factor 2 (RUNX2) interaction partners

1. These data also indicate that MGP is under dual regulation by runx2 through the use of various isoforms and context-dependent formation of transcriptional complexes.

Pig (Porcine) Runt-Related Transcription Factor 2 (RUNX2) interaction partners

1. Klotho gene deficiency promotes high-fat diet-induced fibrosis in aortic valves, likely through the AMPKalpha-RUNX2 pathway.